[THE CINERADIOGRAPHIC METHOD OF STUDYING THE TIME OF PULMONARY CIRCULATION].
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Angiography↗
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Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo.
The objective of this study was to investigate the role of endogenous nitric oxide, formed from L-arginine, in the regulation of pulmonary circulation in vivo, with special reference to the hypoxic pressor response. In artificially ventilated open-chest rabbits, pulmonary vascular resistance at normoxic ventilation (FIO2 = 21%) was 78 +/- 16 cmH2O ml-1 min 1000-1 (mRUL). Hypoxic ventilation (FIO2 = 10%) increased pulmonary vascular resistance to 117 +/- 17 mRUL. N omega-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase, increased pulmonary vascular resistance at normoxic ventilation to 192 +/- 28 mRUL and during hypoxic ventilation to 462 +/- 80 mRUL. During N omega-nitro-L-arginine methylester infusion there was also an increase in mean arterial blood pressure as well as a decrease in cardiac output that was even more pronounced during hypoxic ventilation. L-arginine reversed the effect of N omega-nitro-L-arginine methylester on pulmonary vascular resistance at normoxic ventilation to 140 +/- 26 mRUL and at hypoxic ventilation to 239 +/- 42 mRUL. In spontaneously breathing closed-chest rabbits, N omega-nitro-L-arginine methylester evoked a marked decrease in arterial PO2 and increases in respiration frequency and central venous pressure, while blood pH, PCO2 and base excess remained unchanged. Taken together these findings indicate that endogenous nitric oxide, formed from L-arginine, might be a regulator of ventilation-perfusion matching at normoxic ventilation, and that nitric oxide acts as an endogenous modulator of the hypoxic pressor response.
Amino Acid Oxidoreductases↗
A new physiologic correction technique for re-establishment of pulmonary circulation. Experimental surgical development.
A new physiologic technique is presented for surgical correction of truncus arteriosus, pseudotruncus, transposition of the great arteries, double right ventricular outflow tract with subpulmonary ventricular septal defect and certain cases of Fallot's tetralogy. The basis of the technique are creation of a neo-right atrium, neo-pulmonary trunk, neo-right atrioventricular valve and a neo-pulmonary valve by right angular atriotomy and insertion of a homologous pericardial patch with a monocuspid valve. The pulmonary circulation is re-established by anastomosis of the neo-pulmonary trunk to the pulmonary tree. The technique was used on 26 mongrel dogs. In 14 the experiments were preliminary, to evaluate the technique's validity, and in the other 12 it was performed with extracorporeal circulation and the hemodynamic status was studied at 30 and 180 min postoperatively. The technique and its results and potential advantages are described. Clinical application is considered to be feasible.
Anastomosis, Surgical↗
Historical development of the concept of a pulmonary circulation.
Philosophical speculations and theories regarding the flow of blood through the lungs are reviewed from an historical standpoint. Michael Servetus (1511-1553) described the pulmonary circulation in his book 'Christianismi Restitutio', published in 1553. From manuscripts that were rediscovered and translated in 1924 we now know that Ibn al-Nafis (1210-1288) of Damascus had made the same observations three centuries earlier.
Greece↗
Oral prostaglandin E2 in ductus-dependent pulmonary circulation.
Prostaglandin E2 (PGE2) was administered orally, in doses of 12-65 microgram/kg at intervals of 1-4 hours, to 12 neonates in whom the pulmonary circulation depended on patency of the ductus arteriosus. After an oral dose, both oxygen saturation (SaO2) and plasma PGE2 concentration increased consistently within 15-30 minutes, reaching values comparable to those during i.v. infusions. Treatment continued for 5 days to 4 months. In eight infants, PGE2 withdrawal resulted in a decrease of SaO2, from a mean of 75 +/- 7% to 57 +/- 10% (+/- SD). The ductus remained responsive for long periods--in four infants, for over 3 months. Consequently, surgery could be delayed until the infants and their pulmonary arteries had grown. Side effects during oral therapy were similar to those during i.v. infusion but were less severe in this series. The effectiveness and simplicity of oral PGE2 administration have advantages over i.v. administration, especially for long-term treatment.
Administration, Oral↗
Temporal correlation-based dynamic contrast-enhanced MR imaging improves assessment of complex pulmonary circulation in congenital heart disease.
A temporal correlation (TC) mapping method is proposed to help bolus chasing during dynamic contrast-enhanced (DCE) MRI of complex pulmonary circulation (CPC) in patients with congenital heart disease. DCE-MRI was performed on five healthy male subjects (23-24 years old) and 25 patients (nine males and 16 females, 0.25-44 years old), and TC maps were generated by performing pixel-based computation of cross-correlations to the pulmonary artery with a series of time shifts in all subjects. Qualitative and quantitative evaluations were performed in comparison with original DCE images. TC maps exhibited a better signal-to-noise ratio (SNR) by factors of 4.3 and 1.3 in the lung parenchyma, pulmonary veins, and superior artery/vein; a better intraparenchymal contrast-to-noise ratio (CNR) by factors of 1.5-5.4; and a significantly higher conspicuity in all regions except the pulmonary arteries when graded with a five-point score. TC maps evaluated by two experienced clinicians significantly added relevant information (P<0.001), and in some cases affected the final diagnosis. We conclude that TC maps facilitate bolus chasing for DCE-MRI by reducing recirculation effects and interframe fluctuations, and hence complements morphological imaging of CPC in patients with complex congenital heart disease.
Adolescent↗
[Effects of L-arginine on pulmonary circulation and cerebral blood flow in acute and chronic hypoxic rats].
The effects of L-arginine (L-Arg) on pulmonary circulation and cerebral blood flow in acute and chronic hypoxic rats and their mechanism were studied. The results showed that bolus injection of L-Arg 400mg.kg-1 did not inhibit acute hypoxic pulmonary vasoconstriction (HPV), while 800mg.kg-1 could inhibit HPV. Neither of these two doses of L-Arg was found to have any influence on the change in cerebral blood flow during acute hypoxia. Long-term administration of L-Arg (300mg.kg-1/d) could attenuate chronic hypoxic pulmonary hypertension, the increase in pulmonary vascular resistance and right ventricular hypertrophy, and the HPV as well. It did not influence the cerebral blood flow. Since the inhibitor of NO synthetase, NG-nitro-L-arginine methyl ester, could antagonize the effect of L-Arg, it is suggested that an increase in the synthesis of NO might contribute to the effect of L-Arg.
Animals↗
[Differences of Angiotensin II receptor expression between systemic and pulmonary circulation in children with left-to-right shunt congenital cardiac lesions].
OBJECTIVE: It has been shown that angiotensin converting enzyme inhibitors (ACEI) can reduce the ratio of pulmonary and systemic circulation blood flow (Qp/Qs) and thus decrease the blood flow of left-to-right shunt in children with left-to-right shunt congenital cardiac lesions. This suggests that there are differences in the expression of Angiotensin II receptors between systemic and pulmonary circulation. This study aimed to explore the differences of Angiotensin II receptors type 1 and type 2 (AT1 and AT2 receptors) expression between systemic and pulmonary circulation in children with left-to-right shunt congenital cardiac lesions. METHODS: Lung and skeletal muscular tissues were obtained from 20 children with left-to-right shunt congenital cardiac lesions by biopsy during operation. The specimens were stained by immunohistochemistry techniques for AT1 and AT2 receptors. The technique of morphometric analysis was used to measure the immunoreactivity of AT1 and AT2 receptors (expressed by IOD values) of pulmonary, skeletal muscular and pleural small vascular wall the diameter of which was 15-100 microm. RESULTS: The immunoreactivities of AT1 and AT2 receptors of pulmonary small vascular walls [(124 +/- 95)x10(3) and (85 +/- 62)x10(3) respectively] were significantly lower than those of skeletal muscular [(219 +/- 156)x10(3) and (155 +/- 139)x10(3) respectively] and those of pleural small vascular walls [(279 +/- 191)x10(3) and (175 +/- 128)x10(3) respectively] in children with left-to-right shunt congenital cardiac lesions (P < 0.05). CONCLUSIONS: The expression of AT1 and AT2 receptors in small vascular walls of systemic circulation was higher than that of pulmonary circulation in children with left-to-right shunt congenital cardiac lesions.
Child↗
Structural alterations to the pulmonary circulation in fulminant hepatic failure.
Like patients with chronic liver disease, those with coma due to fulminant hepatic failure may show arterial hypoxaemia even in the absence of pulmonary complications, and in both it is attributed to increased intrapulmonary arteriovenous admixture. This study is concerned with the structural alterations in the pulmonary circulation of patients who have died from fulminant hepatic failure. Precise quantitative morphometric techniques applied to the injected and inflated lung have shown the major abnormality to be a diffuse dilatation of the pulmonary vascular bed affecting arteries and veins of all structural types. At an intra-acinar level the diameter of arteries accompanying respiratory bronchioles was 232.97 micron (+/-SD 46.35) compared with 177.76 micron (+/-SD 30.43) in controls (P less than 0.01). In two-thirds of the patients pleural spider naevi were seen and, throughout the lung, similar significant dilatation of precapillary vessels; but in only one patient were precapillary anastomoses shown. While intrapulmonary venous admixture undoubtedly contributes to hypoxia in fulminant hepatic failure, its exact relation to the structural changes is not yet determined.
Adolescent↗
[18,19,20-trinor-17-cyclohexyl-13,14-dehydro PGF 2 alpha methylester as the cause of hypertension in pulmonary circulation].
The hemodynamic effects of a synthetic compound of PGF 2 alpha have been studied before and after vagosympathectomy. Synthetic PGF 2 alpha caused a marked hypertension in the pulmonary circulation linked with the vasoconstrictor action of this substance on the small lung vessels. A slight hypotension was observed in the denervated animal where the highest values of pulmonary pressure were reached. The authors conclude that this fact may be due to an inhibition of the vasoconstrictor systemic tone secondary to the pulmonary hypertensive state.
Animals↗
Vasodilator response to dopamine in the ferret pulmonary circulation.
1. The isolated perfused lung of the ferret was used to study the effects of dopamine receptor agonists and antagonists. Under constant flow, a fall in pulmonary artery pressure reflects a vasodilator response. Since tone is normally low, agonists were given during hypoxic pulmonary vasoconstriction to enable detection of dilator responses. 2. Vasodilator responses were produced by bolus doses of dopamine over the range 0.1 to 5.0 micrograms kg-1, and by the selective DA1 agonist SK&F 38393 (1-phenyl-7,8-dihydroxy-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride). 3. The dopamine response was blocked by low doses of the selective DA1-antagonist SCH23390 (R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7- ol maleate), and by sulpiride. 4. The vasodilator response to the relatively selective DA2-agonist N,N-di-n-propyl dopamine occurred only at high dose and was incompletely blocked by the selective DA2 antagonist domperidone at a cumulative dose of 10 mg kg-1. 5. Thus dopamine receptors of the DA1 type may mediate vasodilatation in the ferret pulmonary circulation, but no evidence was obtained for the existence of DA2-receptors.
Animals↗
Calcium, mitochondria and oxygen sensing in the pulmonary circulation.
A key event in hypoxic pulmonary vasoconstriction (HPV) is the elevation in smooth muscle intracellular Ca2+ concentration. However, there is controversy concerning the source of this Ca2+, the signal transduction pathways involved, and the identity of the oxygen sensor. Although there is wide support for the hypothesis that hypoxia elicits depolarisation via inhibition of K+ channels, and thus promotes Ca2+ entry through L-type channels, a significant number of studies are inconsistent with this mechanism being either the sole or even major means by which Ca2+ is elevated during HPV. There is strong evidence that intracellular Ca2+ stores play a critical role, and voltage-independent Ca2+ entry mechanisms including capacitative Ca2+ entry (CCE) have also been implicated. There is renewed interest in the role of mitochondria in HPV, both in terms of modulators of Ca2+ homeostasis per se and as oxygen sensors. There is however considerable uncertainty concerning the mechanisms involved in the latter, with proposals for changes in redox couples and both an increase and decrease in mitochondrial production of reactive oxygen species (ROS). In this article we review the evidence for and against involvement of such mechanisms in HPV, and propose a model for the regulation of intracellular [Ca2+] in pulmonary artery during hypoxia in which the mitochondria play a central role.
Animals↗
The adrenomedullin receptor acts as clearance receptor in pulmonary circulation.
Adrenomedullin (AM) is a powerful pulmonary vasodilator with antimitogenic properties. We investigated the role of the AM receptor (AMR) and the calcitonin gene-related peptide type-1 receptor (CGRP1R) in regulating pulmonary vascular AM levels. The AMR antagonist hAM(22-52) (120 nmol/L) significantly elevated AM release compared with controls to 250% after 2 h in isolated rat lungs and to 830% after 4 h in pulmonary artery endothelial cells (PAEC). CGRP1R blockade had no effect. AMR blockade did not influence prepro-AM mRNA levels nor did inhibition of protein synthesis by cycloheximide (0.01 mg/mL) abolish the effect of the AMR antagonist. Radioligand-binding studies with PAEC membranes revealed a decrease by 44% of the AMR density in response to AMR antagonism. Altogether, the pulmonary vascular AMR represents not only a functionally active, but also a clearance receptor; its expression is constitutively stimulated by basal AM. This identifies a novel mechanism for controlling pulmonary AM levels.
Adrenomedullin↗
Effects of nociceptive stimuli on the pulmonary circulation in the ovine fetus.
The fetus is able to exhibit a stress response to painful events, and stress hormones have been shown to modulate pulmonary vascular tone. At birth, the increased level of stress hormones plays a significant role in the adaptation to postnatal life. We therefore hypothesized that pain may alter pulmonary circulation in the perinatal period. The hemodynamic response to subcutaneous injection of formalin, which is used in experimental studies as nociceptive stimulus, was evaluated in chronically prepared, fetal lambs. Fetal lambs were operated on at 128 days gestation. Catheters were placed into the ascending aorta, superior vena cava, and main pulmonary artery. An ultrasonic flow transducer was placed around the left pulmonary artery. Three subcutaneous catheters were placed in the lambs' limb. The hemodynamic responses to subcutaneous injection of formalin, to formalin after fetal analgesia by sufentanil, and to sufentanil alone were recorded. Cortisol and catecholamine concentrations were also measured. Pulmonary vascular resistances (PVR) increased by 42% (P < 0.0001) after formalin injection. Cortisol increased by 54% (P = 0.05). During sufentanil infusion, PVR did not change significantly after formalin. Cortisol increased by 56% (P < 0.05). PVR did not change during sufentanil infusion. Norepinephrine levels did not change during any of the protocols. Our results indicate that nociceptive stimuli may increase the pulmonary vascular tone. This response is not mediated by an increase in circulating catecholamine levels. Analgesia prevents this effect. We speculate that this pulmonary vascular response to nociceptive stimulation may explain some hypoxemic events observed in newborn infants during painful intensive care procedures.
Analgesics, Opioid↗
[Pulmonary circulation and autonomic nervous system].
The function of the autonomic innervation of the pulmonary vasculature remains incompletely understood. Recent studies have contributed to a better understanding of pressure-flow relationships within the pulmonary circulation in intact dog experimental models. This methodological approach has been used to show that, in normal hyperoxic or moderately hypoxic lungs, the sympathetic nervous system exerts a net vasodilatating effect, while the parasympathetic nervous system does not seem to participate to the regulation of vasomotor tone. These results underscore that research in "traditional" physiology still is implicated in ongoing progress in physiopathology and therapeutics.
Animals↗
Fate of prostaglandins E(1) and A(1) in the human pulmonary circulation.
It is recognized that the lung extracts norepinephrine and 5-hydroxytryptamine from the pulmonary circulation and that this process is affected by cardiopulmonary bypass. Since alterations in the lung's processing of vasoactive substances may be a mechanism of pulmonary injury sustained during operation, we investigated the lung's ability to extract or metabolize prostaglandin A1 (ga1) and prostaglandin E1 (PGE 1). Sixteen patients undergoing cardiac surgery were studied. In five patients, just before going on bypass, a 10 ml of blood was withdrawn at a constant rate, simultaneously from the pulmonary artery and left atrium. In 11 patients, 3H-PGE1 was injected just prior to bypass and, in five of these, again after coming off bypass. Extraction was calculated from tritium activity in the samples. Metabolites were quantitated by thin-layer chromatography after being identified by marker compounds run simultaneously in each chromatogram. The pulmonary extraction of PGA1 was 11.3 +/- 2.3% and there were no detectable metabolites in left atrial blood. Before bypass the extraction of PGE1 was 42.3 +/- 14.3% and after bypass 24.8 +/- 10.0% (P less than 0.005; Student's paired t test). PGE1 was extensively metabolized with 79.7 +/- 7.1% of total radioactivity appearing in the left atrium as metabolites before bypass and 89.1 +/- 2.0% appearing after bypass. This study indicates that PGA(1) is not metabolized by the lung and is only slightly extracted. On the other hand, PGE(1) is extensively extracted and metabolized. While the rate of metabolism is not significantly affected by cardiopulmonary bypass, the extractiom before bypass was significantly greater than after bypass.
Adult↗
Flow-volume characteristics in the pulmonary circulation.
Isolated ferret and canine lungs were used to validate a method for assessing determinants of vascular volume in the pulmonary circulation. With left atrial pressure (Pla) constant at 5 mmHg, flow (Q) was raised in steps over a physiological range. Changes in vascular volume (delta V) with each increment in Q were determined as the opposite of changes in perfusion system reservoir weight or from the increase in lung weight. At each level of Q, the pulmonary arterial and left atrial cannulas were simultaneously occluded, allowing all vascular pressures to equilibrate at the same static pressure (Ps), which was equal to the compliance-weighted average pressure in the circulation before occlusion. Hypoxia (inspired PO2 25 Torr) in ferret lungs, which causes intense constriction in arterial extra-alveolar vessels, had no effect on the slope of the Ps-Q relationship, interpreted to represent the resistance downstream from compliance (control 0.025 +/- 0.006 mmHg.ml-1.min, hypoxia 0.030 +/- 0.013). The Ps-axis intercept increased from 8.94 +/- 0.50 to 13.43 +/- 1.52 mmHg, indicating a modest increase in the effective back-pressure to flow downstream from compliant regions. The compliance of the circulation, obtained from the slope of the relationship between delta V and Ps, was unaffected by hypoxia (control 0.52 +/- 0.08 ml/mmHg, hypoxia 0.56 +/- 0.08). In contrast, histamine in canine lungs, which causes constriction in veins, caused the slope of the Ps-Q relationship to increase from 0.013 +/- 0.007 to 0.032 +/- 0.006 mmHg.ml-1.min (P less than 0.05) and the compliance to decrease from 3.51 +/- 0.56 to 1.68 +/- 0.37 ml/mmHg (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Graphical analysis of drug effects in the dog heart-lung preparation--with particular reference to the pulmonary circulation and effects of norepinephrine and 5-hydroxytryptamine.
Our new method for the graphical analysis of drug effects in the dog heart-lung preparation was extended to pulmonary circulation. The equilibrium points, at which the cardiac output (CO) curve and venous return (VR) curve cross each other in the right atrial pressure (RAP)-CO and left atrial pressure (LAP)-CO relations, were directly recorded on two X-Y recorders. The VR curves were obtained by inducing cardiac fibrillation and simultaneously occluding the pulmonary arterial trunk. The competence test, which was utilized previously for recording the CO curve in the RAP-CO relation (Ishikawa et al., 1978), was confirmed to be a good procedure for the CO curve in the LAP-CO relation. During the competence test, the mean pulmonary pressure (Pmp) which is the intercept of the pulmonary VR curve on the LAP axis in the LAP-CO relation was changed as much as the change in the systemic reservoir blood level, with little change in the slope of the pulmonary VR curve. When the reservoir blood level was 100 mm above the superior vena cava and the aortic pressure was 70 mmHg (control), the Pmp value was 136 +/- 7 mmH2O (n = 24). The slope of the pulmonary VR curve was not so different from that of the systemic VR curve in RAP-CO relation. Raising aortic pressure to 100 mmHg caused a shift of the equilibrium point to the right and slightly downwards, increased the Pmp value by 42.9 +/- 9.9 mmH2O (delta Pmp) and decreased the reservoir blood volume by 26.2 +/- 6.4 ml (delta V). The ratio delta V/delta Pmp was 0.66 +/- 0.11 ml/mmH2O. The continuous infusion of norepinephrine 4 micrograms/min caused a shift of the equilibrium point to the left and upwards, decreased the Pmp value by 67.1 +/- 19.1 mmH2O and increased the reservoir blood volume by 35.3 +/- 7.2 ml. The ratio delta V/delta Pmp was 0.56 +/- 0.16 ml/mmH2O. The continuous infusion of 5-hydroxytryptamine at the rate of 60 micrograms/min caused a shift of the equilibrium point almost vertically and downwards, increased Pmp value by 34.8 +/- 3.2 mmH2O and decreased the reservoir blood volume by 45.8 +/- 10.1 ml. The ratio delta V/delta Pmp was 0.88 +/- 0.10 ml/mmH2O.
Animals↗